scholarly journals Inflammation and Oxidative Stress via Persistent Hyperglycemia in Progression of Diabetic Nephropathy in Type 2 Diabetes Mellitus

2013 ◽  
Vol 3 (1) ◽  
pp. 1-4 ◽  
Author(s):  
D Kafle ◽  
N Islam ◽  
B Aryal ◽  
P Adhikary ◽  
Neelina Singh
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Diabetic Nephropathy ◽  
Epithelial Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tubular Epithelial Cells ◽  
Oxidative Stress Biomarkers ◽  
Diabetic Kidney

Diabetic nephropathy is a major microvascular complication of diabetes, representing the leading cause of end stage renal disease in the world, and a major cause of morbidity and mortality in type 2 diabetic subjects. In the kidney, a number of pathways that generate reactive oxygen species (ROS) such as glycolysis, specific defects in the polyol pathway, uncoupling of nitric oxide synthase, xanthine oxidase, NAD (P) H oxidase, and advanced glycation have been identified as potentially major contributors to the pathogenesis of diabetic kidney disease. Changes in oxidative stress biomarkers, including super­oxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins have been associated with diabetic nephropathy due to oxidative stress induced hyperglycemia. Oxidative stress in diabetes is responsible for endothelial dysfunction releasing inflammatory markers cytokines from the damaged renal tissue. Hyperglycemia induces intracellular reactive oxygen species in mesan­gial and tubular epithelial cells which induces cytokines, IL-6 and TNF-α production in glomerular mesangial and tubular epithelial cells in diabetic kidney. Antioxidants inhibit high glucose induced transforming growth factors and extra cellular matrix expression in glomerular mesangial and tubular epithelial cells, which ameliorate features of diabetic nephropathy, suggesting that oxidative stress plays an important role in diabetic renal injury causing diabetic nephropathy. Journal of Chitwan Medical College 2013; 3(1): 1-4 DOI: http://dx.doi.org/10.3126/jcmc.v3i1.8456

Regulatory mechanism of ulinastatin on autophagy of macrophages and renal tubular epithelial cells

2018 ◽  
Vol 16 (1) ◽  
pp. 298-305
Author(s):  
Ming Wu ◽  
Min Hu ◽  
Huansheng Tong ◽  
Junying Liu ◽  
Hui Jiang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Renal Cell ◽  
Reactive Oxygen ◽  
Whole Body ◽  
Inflammatory Factors ◽  
Oxygen Species ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular

AbstractKidney ischemia and hypoxia can cause renal cell apoptosis and activation of inflammatory cells, which lead to the release of inflammatory factors and ultimately result in the damage of kidney tissue and the whole body. Renal tubular cell and macrophage autophagy can reduce the production of reactive oxygen species (ROS), thereby reducing the activation of inflammatory cytoplasm and its key effector protein, caspase-1, which reduces the expression of IL-1β and IL-18 and other inflammatory factors. Ulinastatin (UTI), as a glycoprotein drug, inhibits the activity of multiple proteases and reduces myocardial damage caused by ischemia-reperfusion by upregulating autophagy. However, it can be raised by macrophage autophagy, reduce the production of ROS, and ultimately reduce the expression of inflammatory mediators, thereby reducing renal cell injury, promote renal function recovery is not clear. In this study, a series of cell experiments have shown that ulinastatin is reduced by regulating the autophagy of renal tubular epithelial cells and macrophages to reduce the production of reactive oxygen species and inflammatory factors (TNF-α, IL-1β and IL-1), and then, increase the activity of the cells under the sugar oxygen deprivation model. The simultaneous use of cellular autophagy agonists Rapamycin (RAPA) and ulinastatin has a synergistic effect on the production of reactive oxygen species and the expression of inflammatory factors.

scholarly journals Diabetes Mellitus Directs NKT Cells Toward Type 2 and Regulatory Phenotype / Diabetes Melitus Usmerava Diferencijaciju NKT Celija U Pravcu Tip 2 I Regulatornog Fenotipa

2016 ◽  
Vol 17 (1) ◽  
pp. 35-41
Author(s):  
Nevena Gajovic ◽  
Ivan Jovanovic ◽  
Aleksandar Ilic ◽  
Nevena Jeremic ◽  
Vladimir Jakovljevic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Nkt Cells ◽  
Diabetic Patients ◽  
Oxygen Species ◽  
Chronic Disorder ◽  
Functional Phenotype

Abstract Diabetes mellitus is chronic disorder characterized by hyperglycaemia. Hyperglycaemia induces mitochondrial dysfunction, enhances oxidative stress and thus promotes reactive oxygen species (ROS) production. Earlier studies suggested that reactive oxygen species (ROS) are involved in the pathogenesis of many diseases. Previous studies have revealed that hyperglycaemia changes the functional phenotype of monocytes, macrophages, neutrophils, NK cells and CD8+ T cells. The aim of this study was to investigate whether diabetes affects the functional phenotype of NKT cells. Diabetes mellitus was induced in BALB/c mice by intraperitoneal injection of streptozotocin at a single dose of 170 mg/kg body weight. The number and functional phenotype of splenic NKT cells was assessed by fl ow cytometry, 28 days after diabetes induction. The diabetic condition facilitated the production of antioxidant enzymes, including catalase (p<0.05) and superoxide dismutase. Hyperglycaemia enhanced oxidative stress and thus decreased the number of splenic NKT cells but did not change the percentage of splenic CD3+CD49+ NKT cells that express the activatory receptor NKP46 or produce IFN-γ. However, hyperglycaemia increased the frequency of splenic NKT cells that express KLRG-1 and produce TGF-β, IL-4, and IL-5, and it decreased the frequency of IL-17+ NKT cells. Our study indicates that diabetes mellitus induces oxidative stress and switches the functional phenotype of NKT cells towards type 2 (IL-4 and IL-5 producing NKTs) and regulatory (TGF-β Thproducing NKTs) phenotypes. These findings are correlated with the clinical observation in humans that diabetic patients are more prone to infections and tumours.

scholarly journals Effect of Indoxyl Sulfate on the Repair and Intactness of Intestinal Epithelial Cells: Role of Reactive Oxygen Species’ Release

2019 ◽  
Vol 20 (9) ◽  
pp. 2280 ◽  
Author(s):  
Simona Adesso ◽  
Marco Ruocco ◽  
Shara Francesca Rapa ◽  
Fabrizio Dal Piaz ◽  
Biagio Raffaele Di Iorio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cell Monolayer ◽  
Reactive Oxygen ◽  
Indoxyl Sulfate ◽  
Uremic Toxin ◽  
Oxygen Species ◽  
Intestinal Epithelial

Chronic kidney disease (CKD) is characterized by an oxidative stress status, driving some CKD-associated complications, even at the gastrointestinal level. Indoxyl Sulfate (IS) is a protein-bound uremic toxin, poorly eliminated by dialysis. This toxin is able to affect the intestinal system, but its molecular mechanism/s in intestinal epithelial cells (IECs) remain poorly understood. This study’s aim was to evaluate the effect of IS (31.2–250 µM) on oxidative stress in IEC-6 cells and on the intactness of IECs monolayers. Our results indicated that IS enhanced oxidative cell damage by inducing reactive oxygen species (ROS) release, reducing the antioxidant response and affecting Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation as well its related antioxidant enzymes. In the wound healing assay model, IS reduced IEC-6 migration, slightly impaired actin cytoskeleton rearrangement; this effect was associated with connexin 43 alteration. Moreover, we reported the effect of CKD patients’ sera in IEC-6 cells. Our results indicated that patient sera induced ROS release in IEC-6 cells directly related to IS sera content and this effect was reduced by AST-120 serum treatment. Results highlighted the effect of IS in inducing oxidative stress in IECs and in impairing the intactness of the IECs cell monolayer, thus significantly contributing to CKD-associated intestinal alterations.

scholarly journals The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

2016 ◽  
Vol 397 (8) ◽  
pp. 709-724 ◽  
Author(s):  
José Pedro Castro ◽  
Tilman Grune ◽  
Bodo Speckmann
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Reactive Oxygen ◽  
Whole Body ◽  
Oxygen Species ◽  
Body Energy

Abstract White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho)physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e.g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.

scholarly journals Differential expression pattern of genes involved in oxygen metabolism in epithelial oviductal cells during primary in vitro culture

2019 ◽  
Vol 7 (2) ◽  
pp. 66-76
Author(s):  
Katarzyna Stefańska ◽  
Sandra Knap ◽  
Magdalena Kulus ◽  
Ievgenia Kocherova ◽  
Piotr Celichowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
In Vitro Culture ◽  
Cellular Response ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Female Reproductive Tract ◽  
Oxygen Species

AbstractOxygen metabolism is crucial in establishing successful pregnancy, since excessive amount of reactive oxygen species (ROS) may exert deleterious effects on the developing embryo. There are several defense mechanisms against oxidative stress in the female reproductive tract, including production of antioxidant enzymes by oviductal epithelial cells (OECs). Undoubtedly, OECs play major part in female fertility and may also serve as an in vitro model of the oviduct. Therefore, the aim of this study was to investigate the expression of genes involved in oxygen metabolism. We have isolated OECs from oviducts of crossbred gilts (n=45) and maintained their in vitro culture for 30 days, collecting their RNA at days 1, 7, 15 and 30. The gene expression was determined with the use of Affymetrix® Porcine Gene 1.1 ST Array Strip. Our results revealed 166 differentially expressed genes belonging to four ontology groups: „cellular response to oxidative stress”, “cellular response to oxygen-containing compound”, “cellular response to oxygen levels” and “cellular response to reactive oxygen species”, most of which are also involved in other major processes in the organism. However, our findings provide a valuable insight into porcine reproductive biology and may be utilized in optimization of assisted reproduction techniques.Running title: Genes involved in oxygen metabolism in oviductal epithelial cells

scholarly journals Metallothionein deficiency exacerbates diabetic nephropathy in streptozotocin-induced diabetic mice

2014 ◽  
Vol 306 (1) ◽  
pp. F105-F115 ◽  
Author(s):  
Hiromi Tachibana ◽  
Daisuke Ogawa ◽  
Norio Sogawa ◽  
Masato Asanuma ◽  
Ikuko Miyazaki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Epithelial Cells ◽  
High Glucose ◽  
Tubular Epithelial Cells ◽  
Diabetic Kidney ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
In The Diabetic Kidney

Oxidative stress and inflammation play important roles in diabetic complications, including diabetic nephropathy. Metallothionein (MT) is induced in proximal tubular epithelial cells as an antioxidant in the diabetic kidney; however, the role of MT in renal function remains unclear. We therefore investigated whether MT deficiency accelerates diabetic nephropathy through oxidative stress and inflammation. Diabetes was induced by streptozotocin injection in MT-deficient (MT−/−) and MT+/+ mice. Urinary albumin excretion, histological changes, markers for reactive oxygen species (ROS), and kidney inflammation were measured. Murine proximal tubular epithelial (mProx24) cells were used to further elucidate the role of MT under high-glucose conditions. Parameters of diabetic nephropathy and markers of ROS and inflammation were accelerated in diabetic MT−/− mice compared with diabetic MT+/+ mice, despite equivalent levels of hyperglycemia. MT deficiency accelerated interstitial fibrosis and macrophage infiltration into the interstitium in the diabetic kidney. Electron microscopy revealed abnormal mitochondrial morphology in proximal tubular epithelial cells in diabetic MT−/− mice. In vitro studies demonstrated that knockdown of MT by small interfering RNA enhanced mitochondrial ROS generation and inflammation-related gene expression in mProx24 cells cultured under high-glucose conditions. The results of this study suggest that MT may play a key role in protecting the kidney against high glucose-induced ROS and subsequent inflammation in diabetic nephropathy.

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